The identity and topographic localization of immunocompetent cells and the alteration of cellular markers on ocular resident cells in animals with various experimental uveitis were analyzed by immunohistochemistry, in situ hybridization, and polymerase chain reaction (PCR). Previously, we have demonstrated that T lymphocytes are the predominant infiltrating cells in experimental autoimmune uveoretinitis and experimental melanin-induced uveitis, both macrophages and polymorphonuclear neutrophils are the predominant infiltrating cells in endotoxin-induced uveitis, while all types of leukocytes are present in murine experimental blepharitis. Cytokines and inflammatory mediators play an important role in the immunopathogenesis of ocular inflammation. Expressions of major histocompatibility class (MHC) II antigens and adhesion molecules are observed on ocular resident cells during the inflammatory process. In FY1997 we have identified abundant T helper cell type 1 profile-cytokines and their mRNA in the early stage of autoimmune uveitis in both animal models and human specimens. We have shown that apoptosis plays a regulatory role in limiting ocular inflammation. Fas and Fas ligand are constitutively expressed in the normal cornea, iris, ciliary body, and retina. Alternation of their expression is associated with inflammation and gliofibrosis in human inflammatory eyes. The role of apoptosis is also noted in the development of experimental blepharitis and uveitis. Using microdissection and PCR, we have identified rearrangement of the immunoglobulin heavy chain gene and bcl-2 translocation in primary intraocular lymphoma cells. Elucidating the immunopathological role of the relationship between the infiltrating cells and ocular resident cells will aid in better understanding and management of various ocular diseases in patients.